Nickel potentiates the genotoxic effect of benzo[a]pyrene in Chinese hamster lung V79 cells

Cheng Z. Deng, Michael P. Fons, Judah Rosenblatt, Randa A. El-Zein, Sherif Abdel-Rahman, Thomas Albrecht

Research output: Contribution to journalArticle

10 Citations (Scopus)

Abstract

The modulating effect of acute exposure to NiCl2 on the induction of chromosome aberrations by a model carcinogen, benzo[a]pyrene (B[a]P), was examined in Chinese hamster V79 lung cells. At concentrations up to 20 μg/ml (84.2 μM), NiCl2 did not significantly increase the frequency of chromosome aberrations in V79 cells when the cells were exposed concomitantly to 0.5 μg/ml B[a]P. Addition of the S15 liver microsomal fraction together with the B[a]P did not alter the results. Addition of NiCl2 2 hr before treatment of cells with 0.5 μg/ml B[o]P also did not result in a significant elevation of the frequency of chromosome aberrations, even at NiCl2 concentrations as high as 20 μg/ml. Contrasting sharply with these findings, when V79 cells were treated with NiCl2 immediately after B[a]P exposure, a significant increase in the frequency of chromosome damage was observed at NiCl2 concentrations as low as 5 μg/ml (21.1 μM). NiCl2-mediated enhancement of chromosome damage was also observed when V79 cells were exposed to the reactive B[a]P intermediate, benzo[a]pyrene-r-7,t-8-dihydrodiol-t-9,10-epoxide (BPDE). In the BPDE-treated cells, the level of NiCl2-mediated enhancement was similar to that observed with the tumor promoter 12-o-tetradecanoylphorbol-13- acetate (TPA, 100 ng/ml). These results are consistent with the view that the effect of nickel (II) on B[a]P-induced genetic damage is dependent on the relative times of exposure to Ni2+ and B[a]P. NiCl2 did not enhance the frequency of chromosome aberrations induced by Chromium (VI), regardless of the order of addition of the chemicals to the V79 cells. These results suggest that nickel may act as a promoter of chemically-induced genetic damage through induction of error-prone repair.

Original languageEnglish (US)
Pages (from-to)150-161
Number of pages12
JournalEnvironmental and Molecular Mutagenesis
Volume47
Issue number3
DOIs
StatePublished - Apr 2006

Fingerprint

Benzo(a)pyrene
Chromosomes
Cricetulus
Nickel
pyrene
chromosome
nickel
Aberrations
Lung
7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide
Chromosome Aberrations
damage
Carcinogens
Cells
Epoxy Compounds
carcinogen
tumor
Liver
repair
chromium

Keywords

  • Benzo[a]pyrene
  • Chromosome damage
  • Nickel
  • Potentiation

ASJC Scopus subject areas

  • Environmental Science(all)
  • Environmental Chemistry
  • Genetics
  • Genetics(clinical)
  • Toxicology
  • Health, Toxicology and Mutagenesis

Cite this

Nickel potentiates the genotoxic effect of benzo[a]pyrene in Chinese hamster lung V79 cells. / Deng, Cheng Z.; Fons, Michael P.; Rosenblatt, Judah; El-Zein, Randa A.; Abdel-Rahman, Sherif; Albrecht, Thomas.

In: Environmental and Molecular Mutagenesis, Vol. 47, No. 3, 04.2006, p. 150-161.

Research output: Contribution to journalArticle

Deng, Cheng Z. ; Fons, Michael P. ; Rosenblatt, Judah ; El-Zein, Randa A. ; Abdel-Rahman, Sherif ; Albrecht, Thomas. / Nickel potentiates the genotoxic effect of benzo[a]pyrene in Chinese hamster lung V79 cells. In: Environmental and Molecular Mutagenesis. 2006 ; Vol. 47, No. 3. pp. 150-161.
@article{701530f1a04c41bd94f9a11504cdd796,
title = "Nickel potentiates the genotoxic effect of benzo[a]pyrene in Chinese hamster lung V79 cells",
abstract = "The modulating effect of acute exposure to NiCl2 on the induction of chromosome aberrations by a model carcinogen, benzo[a]pyrene (B[a]P), was examined in Chinese hamster V79 lung cells. At concentrations up to 20 μg/ml (84.2 μM), NiCl2 did not significantly increase the frequency of chromosome aberrations in V79 cells when the cells were exposed concomitantly to 0.5 μg/ml B[a]P. Addition of the S15 liver microsomal fraction together with the B[a]P did not alter the results. Addition of NiCl2 2 hr before treatment of cells with 0.5 μg/ml B[o]P also did not result in a significant elevation of the frequency of chromosome aberrations, even at NiCl2 concentrations as high as 20 μg/ml. Contrasting sharply with these findings, when V79 cells were treated with NiCl2 immediately after B[a]P exposure, a significant increase in the frequency of chromosome damage was observed at NiCl2 concentrations as low as 5 μg/ml (21.1 μM). NiCl2-mediated enhancement of chromosome damage was also observed when V79 cells were exposed to the reactive B[a]P intermediate, benzo[a]pyrene-r-7,t-8-dihydrodiol-t-9,10-epoxide (BPDE). In the BPDE-treated cells, the level of NiCl2-mediated enhancement was similar to that observed with the tumor promoter 12-o-tetradecanoylphorbol-13- acetate (TPA, 100 ng/ml). These results are consistent with the view that the effect of nickel (II) on B[a]P-induced genetic damage is dependent on the relative times of exposure to Ni2+ and B[a]P. NiCl2 did not enhance the frequency of chromosome aberrations induced by Chromium (VI), regardless of the order of addition of the chemicals to the V79 cells. These results suggest that nickel may act as a promoter of chemically-induced genetic damage through induction of error-prone repair.",
keywords = "Benzo[a]pyrene, Chromosome damage, Nickel, Potentiation",
author = "Deng, {Cheng Z.} and Fons, {Michael P.} and Judah Rosenblatt and El-Zein, {Randa A.} and Sherif Abdel-Rahman and Thomas Albrecht",
year = "2006",
month = "4",
doi = "10.1002/em.20179",
language = "English (US)",
volume = "47",
pages = "150--161",
journal = "Environmental and Molecular Mutagenesis",
issn = "0893-6692",
publisher = "Wiley-Liss Inc.",
number = "3",

}

TY - JOUR

T1 - Nickel potentiates the genotoxic effect of benzo[a]pyrene in Chinese hamster lung V79 cells

AU - Deng, Cheng Z.

AU - Fons, Michael P.

AU - Rosenblatt, Judah

AU - El-Zein, Randa A.

AU - Abdel-Rahman, Sherif

AU - Albrecht, Thomas

PY - 2006/4

Y1 - 2006/4

N2 - The modulating effect of acute exposure to NiCl2 on the induction of chromosome aberrations by a model carcinogen, benzo[a]pyrene (B[a]P), was examined in Chinese hamster V79 lung cells. At concentrations up to 20 μg/ml (84.2 μM), NiCl2 did not significantly increase the frequency of chromosome aberrations in V79 cells when the cells were exposed concomitantly to 0.5 μg/ml B[a]P. Addition of the S15 liver microsomal fraction together with the B[a]P did not alter the results. Addition of NiCl2 2 hr before treatment of cells with 0.5 μg/ml B[o]P also did not result in a significant elevation of the frequency of chromosome aberrations, even at NiCl2 concentrations as high as 20 μg/ml. Contrasting sharply with these findings, when V79 cells were treated with NiCl2 immediately after B[a]P exposure, a significant increase in the frequency of chromosome damage was observed at NiCl2 concentrations as low as 5 μg/ml (21.1 μM). NiCl2-mediated enhancement of chromosome damage was also observed when V79 cells were exposed to the reactive B[a]P intermediate, benzo[a]pyrene-r-7,t-8-dihydrodiol-t-9,10-epoxide (BPDE). In the BPDE-treated cells, the level of NiCl2-mediated enhancement was similar to that observed with the tumor promoter 12-o-tetradecanoylphorbol-13- acetate (TPA, 100 ng/ml). These results are consistent with the view that the effect of nickel (II) on B[a]P-induced genetic damage is dependent on the relative times of exposure to Ni2+ and B[a]P. NiCl2 did not enhance the frequency of chromosome aberrations induced by Chromium (VI), regardless of the order of addition of the chemicals to the V79 cells. These results suggest that nickel may act as a promoter of chemically-induced genetic damage through induction of error-prone repair.

AB - The modulating effect of acute exposure to NiCl2 on the induction of chromosome aberrations by a model carcinogen, benzo[a]pyrene (B[a]P), was examined in Chinese hamster V79 lung cells. At concentrations up to 20 μg/ml (84.2 μM), NiCl2 did not significantly increase the frequency of chromosome aberrations in V79 cells when the cells were exposed concomitantly to 0.5 μg/ml B[a]P. Addition of the S15 liver microsomal fraction together with the B[a]P did not alter the results. Addition of NiCl2 2 hr before treatment of cells with 0.5 μg/ml B[o]P also did not result in a significant elevation of the frequency of chromosome aberrations, even at NiCl2 concentrations as high as 20 μg/ml. Contrasting sharply with these findings, when V79 cells were treated with NiCl2 immediately after B[a]P exposure, a significant increase in the frequency of chromosome damage was observed at NiCl2 concentrations as low as 5 μg/ml (21.1 μM). NiCl2-mediated enhancement of chromosome damage was also observed when V79 cells were exposed to the reactive B[a]P intermediate, benzo[a]pyrene-r-7,t-8-dihydrodiol-t-9,10-epoxide (BPDE). In the BPDE-treated cells, the level of NiCl2-mediated enhancement was similar to that observed with the tumor promoter 12-o-tetradecanoylphorbol-13- acetate (TPA, 100 ng/ml). These results are consistent with the view that the effect of nickel (II) on B[a]P-induced genetic damage is dependent on the relative times of exposure to Ni2+ and B[a]P. NiCl2 did not enhance the frequency of chromosome aberrations induced by Chromium (VI), regardless of the order of addition of the chemicals to the V79 cells. These results suggest that nickel may act as a promoter of chemically-induced genetic damage through induction of error-prone repair.

KW - Benzo[a]pyrene

KW - Chromosome damage

KW - Nickel

KW - Potentiation

UR - http://www.scopus.com/inward/record.url?scp=33645510666&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=33645510666&partnerID=8YFLogxK

U2 - 10.1002/em.20179

DO - 10.1002/em.20179

M3 - Article

VL - 47

SP - 150

EP - 161

JO - Environmental and Molecular Mutagenesis

JF - Environmental and Molecular Mutagenesis

SN - 0893-6692

IS - 3

ER -